Haem Flashcards

1
Q

Blood film post splenectomy

A

Howell- Jolly bodies
Pappenheimer bodies
Target cells
Irregular contracted erythrocytes

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2
Q

Fever, chills during blood transfusion

A

Non-haemolytic febrile reaction

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3
Q

Non-haemolytic febrile reaction management

A

Slow or stop the transfusion
Paracetamol
Monitor

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4
Q

Pruritus, urticaria during blood transfusion

A

Minor allergic reaction

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5
Q

Minor allergic reaction management

A

Temporarily stop the transfusion
Antihistamine

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6
Q

Non-haemolytic febrile reaction

A

Thought to be caused by antibodies reacting with white cell fragments in the blood product and cytokines that have leaked from the blood cell during storage

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7
Q

Minor allergic reaction

A

Thought to be caused by foreign plasma proteins

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8
Q

Hypotension, dyspnoea, wheezing, angioedema during blood transfusion

A

Anaphylaxis

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9
Q

blood transfusion anaphylaxis management

A

Stop the transfusion
IM adrenaline
ABC support
oxygen
fluids

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10
Q

blood transfusion anaphylaxis management

A

Stop the transfusion
IM adrenaline
ABC support
oxygen
fluids

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11
Q

Fever, abdominal pain, hypotension during blood transfusion

A

Acute haemolytic reaction

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12
Q

Acute haemolytic reaction management

A

Stop transfusion
Confirm diagnosis
check the identity of patient/name on blood product
send blood for direct Coombs test, repeat typing and cross-matching
Supportive care
fluid resuscitation

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13
Q

Acute haemolytic reaction

A

ABO-incompatible blood e.g. secondary to human error

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14
Q

Pulmonary oedema, hypertension during blood transfusion

A

Transfusion-associated circulatory overload (TACO)

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15
Q

TACO management

A

Slow or stop transfusion
Consider intravenous loop diuretic (e.g. furosemide) and oxygen

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16
Q

TACO

A

Excessive rate of transfusion, pre-existing heart failure

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17
Q

Hypoxia, pulmonary infiltrates on chest x-ray, fever, hypotension during blood transfusion

A

Transfusion-associated acute lung injury (TRALI)

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18
Q

TRALI management?

A

Stop the transfusion

Oxygen and supportive care

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19
Q

TRALI

A

Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood

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20
Q

Warfarin

A

reduction of vitamin K to its active hydroquinone form
* Prolong PT (extrinsic)
* Monitor using INR (as it involve PT and more efficient)
* 2,7,9,10
* War with your gf, she will become ur ex (extrinsic)

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21
Q

Unfractionated heparin

A
  • 9,10,11,12
  • High risk of osteoporosis and HIT
  • Useful in renal failure and where high risk of bleeding (anticoagulation can be terminated rapidly)
  • Protamine sulphate can reverse heparin effect completely
  • Monitor APTT
22
Q

LMWH (dalteparin, enoxaparin)

A
  • 10
  • Low risk of osteoporosis and HIT
  • Not in renal failure
  • Protamine sulphate reverse LMWH partially
  • Monitor factor Xa (as the name RivaroXaban) however frequent monitoring not needed
  • 1st line in VTE prophylaxis and treatment and ACS
23
Q

Platelet transfusion for thrombocytopenia before surgery or an invasive procedure. Aim for plt levels of:

A

> 50×109/L for most patients
50-75×109/L if high risk of bleeding
100×109/L if surgery at critical site

24
Q

Normoblastic causes of macrocytic anaemia

A

alcohol
liver disease
hypothyroidism
pregnancy
reticulocytosis
myelodysplasia
drugs: cytotoxics

25
Q

Megaloblastic causes of macrocytic anaemia

A

Vit B12 deficiency
Folate deficiency (e.g. secondary to methotrexate)

26
Q

Acute intermittent porphyria presentation

A

abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common

27
Q

Acute intermittent porphyria

A

rare autosomal dominant condition caused by a defect an enzyme involved in the biosynthesis of haem

28
Q

Tranexamic acid administration in major haemorrhage

A

IV bolus followed by slow infusion
effective if within 3 hours

29
Q

What medication is contraindicated in T2DM and G6PD deficiency

A

sulphonyureas

30
Q

Extrinsic pathway

A

Activation of TF (tissue factor) and factor VII

31
Q

Intrinsic pathway

A

Factors VIII, IX, XI and XII activation

32
Q

Common pathway

A

Factors V and X activation (converts prothrombin into thrombin)
Where thrombin then converts fibrinogen into fibrin

33
Q

PT what pathway

A

extrinsic

34
Q

APTT what pathway

A

intrinsic

35
Q

Haemophilia A

A

Factor VIII deficiency

36
Q

Haemophilia B

A

Factor IX deficiency

37
Q

Vit K factors

A

II, VII, IX, X

38
Q

APTT and PT in vw

A

normal PT, abnormal APTT, prolonged bleeding time

39
Q

Haemophilia A and B inheritance

A

X-linked recessive

40
Q

Von willebrand disease features

A

Excess or prolonged bleeding from minor wounds
Excess or prolonged bleeding post-operatively
Easy bruising
Menorrhagia
Epistaxis
GI bleeding

41
Q

TTP pentad

A

Fever
Microangiopathic haemolytic anaemia (MAHA)
Thrombocytopaenic purpura
CNS involvement: headache, confusion, seizures
AKI

42
Q

TTP treatment

A

Plasma exchange ASAP
Caplacizumab

43
Q

Factor V leiden cause

A

mutation in clotting factor V, which becomes resistant to inactivation by protein C meaning it won’t turn off clotting

44
Q

Protein C deficiency cause

A

Protein C (and its co-factor, protein S) inactivates clotting factors V and VIII. Inactivating mutations in protein C or S increase the risk of thrombosis

45
Q

Antithrombin III function

A

inhibits factor IIa, Xa, IXa, and XI

46
Q

Alpha thalassaemia presentation

A

Jaundice
Fatigue
Facial bone deformities

47
Q

Alpha thalassaemia management

A

blood transfusions
stem cell transplant
splenectomy

48
Q

Beta thalassaemia minor presentation

A

isolated microcytosis and mild anaemia
typically asymptomatic

49
Q

Beta thalassaemia major presentation

A

Severe symptomatic anaemia at 3-9 months of age when levels of foetal haemoglobin fall
Frontal bossing
Maxillary overgrowth
Extramedullary hematopoiesis (hepatosplenomegaly).

50
Q

Beta thalassaemia management

A

regular blood transfusions
consider iron chelating agent